Pharmacological thrombolysis in Budd Chiari syndrome: a single centre experience and review of the literature

Sharma, Sanchit; Texeira, A; Texeira, P; Elias, Elwyn; Wilde, J. T.; Olliff, Simon

doi:10.1016/j.jhep.2003.09.028

Cited by 111 publications

(63 citation statements)

References 23 publications

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“…The limited amount of available data on thrombolytic therapy found the benefit to be inconclusive. 56 The rationale of angioplasty is to decompress the liver while restoring hepatic blood flow. Luminal strategies to restore blood flow include balloon angioplasty with or without subsequent stenting.…”

Section: Treatmentmentioning

confidence: 99%

Budd‐Chiari syndrome

Martens

Nevens

2015

UEG Journal

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Budd-Chiari syndrome (BCS) is a rare and potentially life-threatening disorder characterized by obstruction of the hepatic outflow tract at any level between the junction of the inferior vena cava with the right atrium and the small hepatic veins. In the West, BCS is a rare hepatic manifestation of one or more underlying prothrombotic risk factors. The most common underlying prothrombotic risk factor is a myeloproliferative disorder, although it is now recognized that almost half of patients have multiple underlying prothrombotic risk factors. Clinical manifestations can be diverse, making BCS a possible differential diagnosis of many acute and chronic liver diseases. The index of suspicion should be very low if there is a known underlying prothrombotic risk factor and new onset of liver disease. Doppler ultrasound is sufficient for confirming the diagnosis, although tomographic imaging (computed tomography (CT) or magnetic resonance imaging (MRI)) is often necessary for further treatment and discussion with a multidisciplinary team. Anticoagulation is the cornerstone of the treatment. Despite the use of anticoagulation, the majority of patients need additional (more invasive) treatment strategies. Algorithms consisting of local angioplasty, TIPS and liver transplantation have been proposed, with treatment choice dictated by a lack of response to a less-invasive treatment regimen. The application of these treatment strategies allows for a five-year survival rate of 90%. In the long term the disease course of BCS can sometimes be complicated by recurrence, progression of the underlying myeloproliferative disorder, or development of post-transplant lymphoma in transplant patients.

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Section: Treatmentmentioning

confidence: 99%

Budd‐Chiari syndrome

Martens

Nevens

2015

UEG Journal

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“…In selected cases thrombolytic therapy was used as an adjunct to these procedures. 8 If there were no suitable hepatic veins for recanalisation found by ultrasound or hepatic venography or if the procedure failed, then we offered TIPS to symptomatic patients to decompress the liver. Our previously described algorithm 6 for treatment of patients with Budd Chiari syndrome was followed in all new patients since 1999.…”

Section: Selection Of Radiological Interventionmentioning

confidence: 99%

Favourable medium term outcome following hepatic vein recanalisation and/or transjugular intrahepatic portosystemic shunt for Budd Chiari syndrome

Eapen

Velissaris²,

Heydtmann³

et al. 2006

Gut

161

126

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Background: We report our experience with management of patients with Budd Chiari syndrome over the past two decades. In 1996 we described a novel approach involving recanalisation of hepatic veins by combined percutaneous and transvenous approaches. This was incorporated into an algorithm published in 1999 in which our preferred treatment for all cases of Budd Chiari syndrome with short segment occlusion or stenosis of the hepatic veins involves recanalisation of the hepatic veins by transvenous or combined percutaneous-transvenous approaches. In symptomatic Budd Chiari syndrome where recanalisation is not possible, we perform transjugular intrahepatic portosystemic shunts (TIPS) because TIPS decompresses the portal circulation directly in an adjustable way. In this series of patients with Budd Chiari syndrome treated with radiological interventions alone, we assess their medium term outcome using two independent objective prognostic indices. Methods: We retrospectively studied 61 patients with non-malignant Budd Chiari syndrome treated by radiological intervention alone in our centre. Results: Actuarial survival for the entire cohort at one year and five years was 94% and 87%, respectively. Survival of our patients with mild disease (according to the Murad classification) was 100% at one year and at five years, with intermediate disease severity 94% at one year and 86% at five years, and with severe disease 85% at one year and 77% at five years. Conclusion: Management of Budd Chiari syndrome by interventional radiology resulted in excellent medium term survival for patients in all categories of disease severity.

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“…The use of catheter-directed therapy has also been emphasized with respect to Budd-Chiari syndrome, and it has been claimed that systemic thrombolytic therapy is not effective for this condition, based on two out of three patients who did not respond. 28 However, there is no anatomic reason why hepatic vein thrombosis should not be amenable to systemic thrombolysis, since this therapy has succeeded with portal vein thrombosis, 27 which may be difficult to access by a catheter approach.…”

Section: Systemic Versus Catheter-administered Tissue Plasminogen Actmentioning

confidence: 99%

“…These agents also have a role in patients who have had arterial cerebral vascular accidents, 21,22 in patients who are in hemodynamic shock from pulmonary emboli, and in patients with venous thrombosis at other sites. [23][24][25][26][27][28]29,30 As for PNH, there have been a number of papers in the literature, [10][11][12][13][14][15][17][18][19]31,32 most of them on isolated cases. Here we report our experience with thrombolytic therapy in a highly selected group of nine patients with PNH, all of whom had severe thrombotic complications, which were regarded as potentially fatal if not treated, or which were progressing despite anticoagulation: in this respect, tissue plasminogen activator (tPA) can be regarded as a second-line treatment for patients with PNH complicated by venous thrombosis.…”

Section: Introductionmentioning

confidence: 99%